|Payment & Shipping Terms||Supply Capacity|
|Unit Price:||1.0 USD||Production Capacity:||5000kg|
|Payment Terms:||Paypal, T/T, WU, Money Gram||Packing:||as your requst|
|Min. Order:||10 Gram||Delivery Date:||after payment 3-7days|
|Test Items||Specification||Test Results|
|Appearance||White crystalline powder||Comply|
|Loss on drying||≤0.5%||0.01%|
Simplified hormone , from the testis or urine extracted with the role of a male hormone steroids,
norethisterone, test propionate in the middle Body, is widely used in small rheumatoid arthritis,
diuretic, and a variety of contraceptive to control infectious inflammation.
Due to its secretion from a number of different glands and its often rapid conversion to other hormones, the control of androstendion within the body is very complex. However, two key parts of the brain (the hypothalamus and pituitary gland) are known to be important in the control of androstendion secretion from the testes, ovaries and adrenal cortex. The release of androstendion by the adrenal cortex is thought to be related to the pituitary gland's secretion of a specialised hormone, adrenocorticotropic hormone. Precisely how adrenocorticotropic hormone and other hormones control the adrenal gland's production of androstendion is, however, unclear. The testes and ovaries are stimulated to release androstenedione by luteinising hormone and follicle stimulating hormone. These are released from the anterior pituitary gland in response to a hormone signal from the hypothalamus.
Boys with too little androstendion may fail to develop the sexual characteristics associated with puberty, including pubic and body hair, growth of the sexual organs and deepening of the voice. Similarly, girls may fail to start their periods and may not undergo many of the changes usually seen in puberty. Additionally, if a male foetus has too little androstendion, he may be born with abnormal genitalia. Too little androstenedione in later life would cause the same changes for both men and women as too little test and oestrogen.
4-Androstenedione can be synthesized in one of two ways. The primary pathway involves conversion of 17-hydroxypregnenolone to by way of 17,20-lyase, with subsequent conversion of to 4-Androstenedione via the enzyme 3-β-hydroxysteroid dehydrogenase. The secondary pathway involves conversion of 17-hydroxyprogesterone, most often a precursor to cortisol, to 4-androstenedione directly by way of 17,20-lyase. Thus, 17,20-lyase is required for the synthesis of 4-androstenedione, whether immediately or one step removed.
The production of adrenal 4-Androstenedione is governed by ACTH, whereas production of gonadal 4-Androstenedione is under control by gonadotropins. In premenopausal women, the adrenal glands and ovaries each produce about half of the total 4-androstenedione(about 3 mg/day). After menopause, 4-androstenedione production is about halved, due primarily to the reduction of the steroid secreted by the ovary. Nevertheless, 4-androstenedione is the principal steroid produced by the postmenopausal ovary.